1. Heart sounds –origin,normal& abnormal
Dolly mathew

2. Brief discrete auditory vibrations charecterized by intensity(loudness),frequency(pitch),& quality
high frequency sounds –
related to opening :OS, ES
Closure sounds-S1,S2
Low frequency sounds - early & late diastolic filling events of the ventricle

4. S1 – 4 sequential components (phono)
Small frequency vibrations, coincides with the beginning of LV contraction- felt to be muscular origin
High frequency M1
High frequency T1
Small frequency vibrations coincides with acceleration of blood into the great vessel

5. First heart sound - M1T1
Sudden tensing of MV leaflet after closure of mitral valve, which sets the surrounding cardiac structures including the blood into vibrations
Complete coaptation of valve leaflets& final tensing are not simultaneous
Final tensing responsible for M1

6. Factors affecting s1 structural integrity of valve :
inadequate coaptation of mitral valve - soft S1 (severe MR )
Loss of leaflet tissue – soft S1 (IE)
thickness & mobility of the valve
In mild- mod MS, the increased LA pressure causes the mobile portions of the mitral valve leaflets to be more widely separated  accentuated M1
The stiff noncompliant leaflets & chordae tendinae appear to resonate with increased amplitude
Calcified mitral valve( long standing MS) immobilizes the valve- soft S1

7. 2. velocity of the valve closure: determined by the position of mitral valve at the onset of ventricular systole
Position of mitral valve is altered by relative timing of atrial & ventricular systole( PR interval )
Long PR longer diastolic filling timeLV pressure gradually increases  mitral valve leaflets slowly drift together  lesser distance between leaflets
Short PR  mitral leaflets are farther apart at the onset of ventricular systole closes with a high velocity large excursion

9. Longer PR( ms)- ventricular contraction accelerate blood towards the AV valve only during the time required to stretch the closed valve to its elastic limit
the rate of ventricular pressure development is negligible & insignificant VA pressure gradient

10. when PR markedly prolonged (>550ms) re opening occurs due to continuing blood inflow from pulmonary arterial to venous bed
The valve is open at the onset of ventricular systole,s1 loud

11. Short PR – valve cusps are in their most divergent position when ventricular contraction begin, ventriculoatrial pressure gradient greater, louder s1
Very short PR- atrial systole coincides with ventricular systole, diminishing the VA gradient at the time of AV valve closure- s1 soft/ inaudible

13. 3. Status of ventricular contraction
Increased myocardial contractility increases the rate of LV pressure(dP/dt) – loud S1
( Exercise, high output state)
Decreased dP/dt – soft S1
(A/c MI, myocarditis)
Loss of isovolumic contraction- decreases dp/dt- decreased velocity of mitral valve closure - soft S1
MR ,large VSD - S1 may be masked by the murmur
- loss of isovolumic contraction
decreased dp/dt

14. 4. Heart rate
Tachycardia- loud s1
Reasons – short PR interval
- wide opened valves due to short diastole
- increased myocardial contractility

15. 5. Transmission characteristics of thoracic cavity & chestwall -Obesity, emphysema,pericardial effusion decrease the intensity of all auscultatory events -Thin chest wall increases the intensity

16. conditions causing Loud S1 (M1)
MS-thickened mobile leaflets, high LA pressure
Interval from LV-LA pressure crossover to mitral valve closure is same as in normal state, rate of ventricular pressure development (dp/dt) during this period is higher
MVP ( non rheumatic MR): holosystolic prolapse – S1 loud- due to delay in checking action of mitral valve caused by increased valve displacement
increased amplitude of leaflet excursion,
summation of normal M1& nonejection click
Exercise – tachycardia induced short PR
-Increased LV contractility
- increased flow across the valve

17. Loud T1 TS ASD - increased tricuspid flow
Anomalous pulmonary venous connection
- increased tricuspid flow

18. Soft S1
MR- decreased mobility, poor coaptation, loss of isovolumic contraction
Some of the energy of ventricular contraction may be spent developing kinetic energy responsible for the regurgitant flow, diminishing the rate of rise of intraventricular pressure
Calcific MS- immobility of mitral valve

19. Severe AR-
- pre closure of mitral valve as a result of rapid increase in the LV filling pressure
In a/c AR, aortic pressure markedly reduced, LV pressure markedly elevated, leading to equilibration of pressure at the onset of LV systole
Since the energy of ventricular contraction is immediately converted into kinetic energy in the form of aortic transvalvular flow, the energy producing the mitral valve displacement is reduced

20. LBBB- delay in onset of LV contraction- delayed M1
- decreased LV contractility
- concomitant 1st degree AV block
- presence of noncompliant LV leading to preclosure of mitral valve
a/c myocardial infarction-
- decreased ventricular contractility,
- associated MR,
-LBBB

21. Variable S1
AF - varying cycle length - varying force of ventricular contraction
S1 intensity & mitral valve closure velocity closely related in AF (Mills& Craige)
With short ventricular cycle lengths AV valve closure may begin during the rapid filling phase of the immediately preceding diastole,during which MV leaflets are relatively divergent, leading to loud S1
If S1 occur after rapid filling phase, intensity is likely to be related to rate of ventricular pressure development
S1 amplitude & rate of pressure development tend to increase with increase in cycle length until a critical length is reached, little changes thereafter
So difficult to relate the observed intensity to the cycle length

22. CHB- varying PR interval- Intermittent loud S1- cannon sound
VT with AV dissociation - varying position of AV valves at ventricular systole
Atrial flutter with varying conduction
Pulsus alternance – regular alternation in the intraventricular pressure development
Electrical alternance- heart is swinging in a pendular arc , whose period is twice the heart rate , ventricular systole occur at each end of the pendular arc
Alternating distance & fluid volume between the source of sound production & chestwall

23. wide splitting S1 Electrical delay(delayed RV contraction)-RBBB
( with normal sequence) LV pacing
- Ectopics from LV
Mechanical delay Ebstein’s anomaly (sail sound due to delayed activation, increased RA pressure)
- TS& RA myxoma ( due to increased RA pressure)
Reverse splittingT1M1- RV pacing( delayed LV contr)
-RV ectopics(delayed LV contr)
-LBBB(delayed LV contr)
- MS, LA myxoma
(Hemodynamically significant mitral valve obstruction can cause reverse splitting, mitral valve closure delayed due to increased LA pressure that must be overcome by rising the LV pressure before closure can occur)

24. Second heart sound High frequency, 120 – 150Hz
Events associated with closure of aortic & pulmonary valves
Sudden deceleration of reterograde bloodflow in the aorta & PA, which sets the entire cardiohemic system into vibrations
A2 louder (higher pressure in aorta) P2 later to (longer RV ET and more HI)
Normal split- <30 ms exp, ms insp
Inspiratory split- P2 delay accounts for 73% & early A2 accounts for27%

25. P2 delay 2/3rd due to increased hangout interval during inspiration, and 1/3rd due to increased RV ejection time
Expiratory split of S2 must be confirmed in sitting position- P2 occurs earlier and the split disappears
Hangout interval
Semilunar valves expected to close at the point of cross over of pressures, however these valves closes slightly later
Hangout interval (30 ms Ao &80ms PA)

27. Factors affecting intensity of A2 / P2
Great artery pressure
Elastic recoil of great artery root- determined primarily by the rate at which stroke volume is ejected
status of Semilunar valve
Size of vessel
Position of vessel

28. Hypertension ( higher pressure in the aorta )
Loud A2-
Hyperkinetic states( increased flow across normal valve)
Hypertension ( higher pressure in the aorta )
Aortic root dilation(increased flow, dilated vessel)
TGA ( Aorta arises more anteriorly )
Loud P2-
Pulmonary hypertension( dilated pulmonary trunk,increased PA pressure)
ASD ( dilated pulmonary trunk, increased flow across the valve)
straight back syndrome( decreased AP diameter)

29. Diminished A2- Valvular AS ( distorted valve ,diminished mobility)
AR (restricted valve mobility, poor coaptation)
Diminished P2
Valvular PS (thickened leaflet, diminished mobility)
Dysplastic valve (distorted valve anatomy& diminished mobility)

30. Inspiration may attenuate P2 due to increased lung interposition
Massive pulmonary embolism-
A2 soft due to decreased cardiac output
P2 loud due to increased PA pressure (may be soft in very large embolus
A2 early, P2 late

31. Wide physiological split
Late P2-
Electrical causes like RBBB (ET)
PS (ET, HI)
ASD (HI, ET, RBBB)
PH + RVF (ET)
IDPA (HI)
Early A2-
Severe MR (decreased LV ET- due to loss of isovolumic contraction)
VSD (decreased LV ET due to loss of isovolumic contraction) )
Pericardial tamponade (ET)
Both- PE
VSD

32. Wide fixed split
When the RV or LV stroke volume doesnot change with inspiration
RVF PE
Simultaneous increase in RV & LV filling- ASD
Delayed P2 due to increased venous return to RV
Delayed A2 due to decreased left to right shunt
No further increase in hi is possible

33. Reversed split S2
Types I, II & III (latter two by phono)
inspiration : single S2(P2A2) / Expiration : P2-A2
Typeii - inspiration :A2-P2 / Expiration : P2-A2
Late A2-
Electrical delay- LBBB(delayed activation LV,prolonged isovolumic contraction time) ,RV pacing, RBBB VPCs,
AS, HOCM(due to large systolic gradient, ?prolonged LV relaxation)
Early P2- TR

34. Single S2 Aging (early P2, delayed A2)
Murmur obscuration (MR, VSD, AS, PS, PDA)
Absent P2 (PS, TOF, PA, TA)
fusionA2-P2
Eisenmenger VSD (same inspiratory delay), single ventricle
Apparently single S2(inaudible P2)-
Emphysema,
obesity,
pericardial effusion

35. S3 Mechanism of production
Impact theory - ventricular filling occurs early in the diastole, if ventricles resist this rapid flow, vibratory activity results which are transmitted to the chest wall
Ventricular theory - sudden cessation of ventricular filling resulting in distension & vibration of ventricular wall, papillary muscles & chordae
Valvar theory- sudden limitation of longitudinal expansion of LV wall during early diastole
Abnormal s3 - altered physical properties of the recipient ventricle &/or increase in the atrioventricular flow during rapid filling phase of ventricle

36. s3 Follows A2 by 140 to 160 msec (physiological 120-200 msec)
Gallop rhythm - auscultatory phenomenon of tripling or quadrupling of heart sounds resembles the canter of a horse

37. Causes of S3 Normal- Diastolic overload states- LVF
Children and young adults
Hyperkinetic states( diastolic overload with high atrial pressure)
Diastolic overload states-
MR(earlier, higher frequency), VSD, PDA
LVF
CCP (earlier, louder, higher pitched, due to rapid rise of LV pressure)

38. Normal S3 disappears in upright position
Abnormal S3 better heard after isotonic exercise, passive leg raising ( augments the venous return & mid diastolic atrio ventricular flow)
RV S3- TR , ASD, CCP

39. S4- atrial gallop- presystolic gallop
The s4 occurs just after atrial contraction and immediately before S1
20 to 30 Hz
caused by stiffening of the walls of the ventricles (usually the left), which produces abnormally turbulent flow as the atria contract to force blood into the ventricle

40. audible in the elderly due to a more rigid ventricle
LVS4 heard best at the cardiac apex
become more apparent with exercise, with the patient in left lateral position in expiration
RVS4 most evident LLSB
louder with exercise, inspiration

41. Absent in chronic MR (poor LA contractility
Present in acute MR (hyperdynamic atrial systole)

42. Causes- CAD, HT, AS, HCM ( decreased ventricular compliance)
acute MR( hyperdynamic atrial systole)
a/c AR (Decreased LV compliance)
AV blocks (prolonged PR ms atrial gallop heard
in addition to s1)
CHB (S4/ summation sound occur randomly in diastole P&QRS relationship is random)
RV S4- PH( increased resistance to ventricular filling)
PS, PE ( RV pressure overload)
S3 & S4- non obstructive AV valve
S4- healthy atrium
S3 has more inspiratory decrease than S4.
Upright posture- physiological S3 & S4 vanishes

43. Systolic ejection sounds
Valvular- arising from deformed valve
vascular or root events - Rapid forceful ejection into great vessels
Coincident with maximal excursion of domed valve when its elastic limits are met
Mechanism - Deceleration of oncoming blood column sets the entire cardiohemic system into vibration
high frequency sound
Intensity of ES correlates directly with mobility of the valve
No correlation with severity of obstruction

44. Ejection sounds Semilunar valve stenosis-
Absent in extremely severe stenosis and in calcification.
Aortic stenosis- common in BAV, less common in acquired valvular AS
Pulmonic stenosis-
Common in valvular PS
Softens or disappears with inspiration
Absent in very mild PS

45. Pulmonary valvular ejection sounds Occurs at maximal excursion of stenotic pulmonary valve

46. Nonejection sounds MVP/TVP a/w systolic regurgitant mr
Caused by tensing of AV valves during systole
Produced by vibrations of the entire cardiohemic system when the elastic limits of prolapsed valve are suddenly reached
Standing – click moves earlier, greater degree of prolapse
Squatting- later prolapse, moves towards s2

47. diastolic sounds - Opening snap
Sharp, high pitched brief early diastolic
60-100ms after A2
Represents the isovolumic relaxation period of the ventricle, inversely proportional to LA pressure
Sudden stoppage of the opening movements of the valve(Margolies & Wolferth theory)
Sudden tensing of the valve leaflets by the chordae tendinae

48. AF- shorter A2-OS with short R-R cycles
-With Longer preceding R-R, the LA pressure falls, A2-OS widens
Stenotic OS-MS,TS
Nonstenotic mitral- MR, ( increased flow,swift opening of nonstenotic valve); VSD( functional OS)
Nonstenotic tricuspid –TR, ASD(functional opening snap), ebstein anomaly( increased flow , rapid excursion)

49. Mild MS A2-OS>120ms mean LAP <5mmHg Moderate MS60-80 ; 5-10MmmHg Severe MS 40-60ms ;>15mmHg

50. Factors affecting OS
Heart rate- tachycardia decreases A2-OS ( shortening of diastole)
Brady increases A2-OS ( prolonged diastole)
Hypertension – A2-OS increased ( LVpressure takes longer time to descend below LAP& early occurance of A2)
Increased LVEDP- increased A2-OS (obliteration of transmitral gradient)

51. Tumour plop;
high frequency heard in atrial myxomas
Abrupt diastolic seating of mobile myxoma within Rt or Lt AV orifice
Later than OS

52. Pericardial knock
Diastolic sound caused by loss of pericardial elasticity that limits ventricular filling
High pitched sound
Louder with inspiration, squatting ( increased venous return)
Mechanism-structural restriction of diastolic filling by the restricting pericardial shell
Disappear following pericardiectomy

53. Prosthetic valve sounds
Mechanical valves
ball-in-cage valve- opening & closing sound
Tilting disc & bileaflet- high pitched metallic closing sound
aortic position: OS analogous to ejection click
Closing sound coincides with S2
Clicks occur during the harsh ESM
Mitral position : opening sound analogous to opening snap
closing sound coincides with S1
tilting disc – closing sounds distinctly heard
(aortic & mitral position)
Bioprosthetic valves- closing sounds are similar to those of native valves
a low frequency early os may be present in mitral position

54. Pacemaker sounds
Occuring nearly synchronously with pacemaker spike
Caused by stimulation of intercostal nerves adjacent to endocardial electrodes
Results in contraction of intercostal muscles

55. Pericardial friction rubs
High pitched, leathery, scratchy sound
Three components
Mediastinal crunch
Scratchy sounds, due to air in the mediastinum,
Most frequently during ventricular systole & in a random fashion

56. Thank you